Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Minihepcidins are hepcidin agonists that have been previously shown to reverse iron overload and improve erythropoiesis in mice affected by non-transfusion dependent thalassemia. Due to their extreme anemia, the previous model of transfusion dependent thalassemia is inadequate to investigate whether Minihepcidins can improve red blood cell quality, lifespan and, ineffective erythropoiesis. To overcome this limitation, we generated a new murine model of transfusion dependent thalassemia with severe anemia and splenomegaly, but sufficient red cells and hemoglobin production to test the effect of Minihepcidins. Furthermore, this new model demonstrates, for the first time, cardiac iron overload. In absence of transfusion, Minihepcidin improved red blood cell morphology and lifespan as well as ineffective erythropoiesis. Administration of Minihepcidin in combination with chronic red blood cell transfusion further improved the ineffective erythropoiesis and splenomegaly and reversed cardiac iron overload. These studies indicate that drugs like Minihepcidins have therapeutic potential for transfusion dependent thalassemia patients.

Original publication




Journal article



Publication Date



Iron Metabolism, Red Cells, Thalassemia